Naito S, Imataka K, Seko Y, Fujii J
Institute for Adult Diseases, Asahi Life Foundation, Tokyo.
J Cardiol Suppl. 1990;23:31-45; discussion 46.
A peculiar mitral periannular cardiac muscle lesion was developed in rabbits with experimentally-induced mitral regurgitation by vagus stimulation. We investigated the cardiac muscle lesion of mitral regurgitation rabbits (MR group, N = 30) using pathohistological, immunohistochemical and biochemical methods. Control group consisted of 21 non-treated rabbits. The periannular cardiac muscle lesion in the MR group was characterized by swelling and increased stiffness of the muscle which were observed as swelling and degeneration of the myocardial cells and interstitial fibrosis on the microscopic observation, and increase in the amount and dimension of collagen tendon, strands, and struts on the scanning electron microscopic study. Hydroxyproline content of the periannular cardiac muscle lesion in the MR group was significantly abundant compared with that in the control group (10.5 +/- 1.6 vs 7.8 +/- 0.9 mg/g.wet wt, mean +/- SD, p less than 0.01) and that of the cardiac muscle in the left ventricular free wall in the MR group (10.5 +/- 1.6 vs 7.1 +/- 0.9, p less than 0.01). Furthermore, the immunohistochemical study clearly indicated that the increased collagen in the periannular cardiac muscle lesion in the MR group was type III collagen. A significant myosin heavy chain isozyme change from V1 myosin to V3 myosin on pyrophosphate gel electrophoresis was observed at the periannular cardiac muscle lesion in the MR group compared with that in the control group (%V1: %V3, 4.2: 92.7 vs 15.4: 74.7, p less than 0.01) and that of the cardiac muscle in the left ventricular free wall in the MR group (4.2: 92.7 vs 14.1: 75.4, p less than 0.01). These results suggested that the mitral periannular cardiac muscle in experimental mitral regurgitation rabbits induced by vagus stimulation suffers a strong mechanical load compared with the cardiac muscle in the left ventricular free wall.
通过迷走神经刺激诱导实验性二尖瓣反流的家兔出现了一种特殊的二尖瓣瓣环心肌病变。我们采用病理组织学、免疫组织化学和生化方法研究了二尖瓣反流家兔(MR组,N = 30)的心肌病变。对照组由21只未处理的家兔组成。MR组的瓣环心肌病变表现为肌肉肿胀和硬度增加,显微镜观察可见心肌细胞肿胀和变性以及间质纤维化,扫描电子显微镜研究显示胶原纤维束、丝和支柱的数量和尺寸增加。MR组瓣环心肌病变的羟脯氨酸含量明显高于对照组(10.5±1.6 vs 7.8±0.9 mg/g湿重,均值±标准差,p<0.01)以及MR组左心室游离壁心肌的羟脯氨酸含量(10.5±1.6 vs 7.1±0.9,p<0.01)。此外,免疫组织化学研究清楚地表明,MR组瓣环心肌病变中增加的胶原蛋白是III型胶原蛋白。与对照组相比,MR组瓣环心肌病变处焦磷酸凝胶电泳显示肌球蛋白重链同工酶从V1肌球蛋白显著转变为V3肌球蛋白(%V1:%V3,4.2:92.7 vs 15.4:74.7,p<0.01),与MR组左心室游离壁心肌相比也有同样变化(4.2:92.7 vs 14.1:75.4,p<0.01)。这些结果表明,与左心室游离壁心肌相比,迷走神经刺激诱导的实验性二尖瓣反流家兔的二尖瓣瓣环心肌承受着更大的机械负荷。